A year ago, the horse-racing world in Australia was plunged into a crisis of nightmarish proportions, as horses began to die from a dreadful, untreatable and previously unknown lung disease. It was a nightmare from which owners, jockeys, trainers and veterinarians have emerged only recently. Yet a worrisome mystery remains. Although scientists have identified the virus responsible for the disease, they don't know where it came from - or whether it might return.

In mid-September 1994, a pregnant mare in Brisbane, Queensland, died after a brief but severe illness with very high fever. The horse's 49- year-old trainer, Victor Rail, and a younger stablehand who had been in close contact with the dying mare, developed symptoms similar to those of severe influenza. The stablehand recovered, but the trainer died after six days in intensive care. A post-mortem showed that he had succumbed to a particularly damaging form of pneumonia.

Meanwhile, several other horses, most of them living near the first victim, had become sick. Over two weeks, 21 horses developed the respiratory disease, which caused distressingly laboured breathing. Fourteen of them either died or were destroyed because of the intensity of their suffering. Vets had little idea what was causing the illness. Fears grew that it might spread to horses and perhaps humans throughout Australia and even abroad.

A team of investigators came together quickly. It included Keith Murray, head of the Commonwealth Scientific and Industrial Research Organisation's Australian Animal Health Laboratory near Melbourne, and Linda Selvey, of the Queensland Health Department in Brisbane. Their first task was to determine whether the deaths had been caused by a chemical (which would mean it could not pass from one animal to another) or (more likely and more disquietingly) by a virus or other microbe.

The investigators transferred tiny quantities of lung tissue from the dead horses and the trainer into laboratory cultures of living cells. They then incubated the cells, hoping to grow any microbe that was present in the tissues. Sure enough, a virus did grow. Examination under the electron microscope suggested that it might belong to the group known as morbilliviruses. This group includes the viruses that cause measles in humans and distemper in dogs. A morbillivirus, previously unknown, was also responsible for the devastating infection that swept through harbour seals in north-west Europe in 1988.

But the mere presence of a morbillivirus in the Brisbane samples did not establish that it had killed the horses and the trainer. To confirm that it had, the investigators had no choice but to inoculate the material into two healthy horses. A little over a week later, both developed a high fever and signs of respiratory distress, and were then humanely killed. Post-mortem tests revealed the morbillivirus throughout their lungs, which had been severely damaged, with haemorrhage and froth in the airways. The horses and the trainer had died literally by drowning - their lungs had filled up with fluid caused by the virus infection.

When Keith Murray and his colleagues reported these findings in the journal Science recently, they were able to provide a detailed description of the microbe that set alarm bells ringing in Australia last year. It looks different from other morbilliviruses, with a double rather than single fringe of projections from its surface. Sophisticated genetic studies have shown that it is only distantly related to the viruses responsible for infections such as measles and distemper.

Soon after the Brisbane incident, the Australian investigators developed a test for antibodies to the microbe, which they termed Equine morbillivirus (EM). They used it to test 1,600 other horses and 90 humans in the vicinity of the outbreak, and found that none was infected. The disease did not, as feared at first, move far from its original location.

Notwithstanding the rapid, skilled and successful detective work that followed last September's horse deaths, and the failure of the virus to spread nationwide, the epidemic had two worrying features. First, EM differs from other morbilliviruses in being able to attack not just a single species but two, including humans. Second, it is obviously extremely virulent, killing about 70 per cent of horses that it infected in the Brisbane outbreak.

The incident leaves one crucial gap in our understanding. Where did EM come from? Is it present, without causing disease, in some other Australian animal? If so, why did it suddenly jump to another species? Until these questions are answered, horse owners will remain anxious that this horrendous and untreatable disease could return.